The stimulus for acetylcholine release is the action potential traveling down the axon of the presynaptic neuron. This depolarization causes calcium channels to open, allowing calcium ions to enter the axon terminal and trigger the release of acetylcholine into the synaptic cleft.
The word cholingeric deals with biology and neurotransmitters. It means that a nerve can be activated by acetylcholine within the sympathetic and parasympathetic branches of the nervous system.
The release of acetylcholine from a synaptic terminal is triggered by the arrival of an action potential at the terminal. This depolarization causes voltage-gated calcium channels to open, leading to an influx of calcium ions into the terminal. The increased calcium levels then trigger the release of acetylcholine vesicles into the synaptic cleft.
Acetylcholine is broken down by the enzyme acetylcholinesterase into acetate and choline. This breakdown process is essential for terminating the action of acetylcholine at the synapse, allowing for proper signaling between nerve cells. Excess acetylcholine breakdown can lead to conditions such as myasthenia gravis.
The antidote for excess acetylcholine is atropine, which acts as a competitive antagonist at cholinergic receptors. Atropine inhibits the effects of acetylcholine by blocking its binding, therefore reversing toxicity symptoms such as bradycardia, bronchoconstriction, and excessive salivation caused by excess acetylcholine.
Synaptic vesicles in the axon terminals of neurons contain acetylcholine. Acetylcholine is a neurotransmitter that is released from these vesicles into the synaptic cleft to transmit signals to target cells or other neurons.
The transmission of the stimulus at the neuromuscular junction involves the release of acetylcholine from the motor neuron, binding to acetylcholine receptors on the muscle cell membrane, causing depolarization of the muscle cell, and ultimately leading to muscle contraction.
acetylcholine
The stimulus that travels from the motor neuron to skeletal muscle is an electrical signal called an action potential. This action potential causes the release of neurotransmitters, specifically acetylcholine, which then stimulates muscle contraction.
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acetylcholine (ACh)
Alpha-Motor neurons release the neurotransmitter acetylcholine at a synapse called the neuromuscular junction. When the acetylcholine binds to acetylcholine receptors on the muscle fiber, an action potential is propagated along the muscle fiber in both directions.
is the release of acetylcholine from the motor neuron into the synaptic cleft.
The axon terminal of a motor neuron releases the neurotransmitter acetylcholine. Acetylcholine is responsible for transmitting signals from the motor neuron to muscle fibers, leading to muscle contractions.
Acetylcholine is the primary chemical transmitter released at the neuromuscular junction. It binds to acetylcholine receptors on the muscle cell membrane, leading to muscle contraction.
Acetylcholine is the excitatory neurotransmitter released by neurons innervating skeletal muscles. Acetylcholine release stimulates muscle contraction by acting at the nicotinic-acetylcholine receptor on the surface of the muscle cell.
The ion needed to initiate the release of acetylcholine into the synaptic cleft is calcium (Ca2+). When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium to enter and trigger the release of acetylcholine-containing vesicles.